Ischemic retinal diseases are the major cause of vision impairment worldwide. Currently, there are no available treatments for ischemia‑induced retinal neurodegeneration. Circular RNAs (circRNAs) have emerged as important regulators of several biological processes and human diseases. The present study investigated the role of circRNA‑ZYG11B (circZYG11B; hsa_circ_0003739) in retinal neurodegeneration. Reverse transcription quantitative polymerase chain reaction (RT‑qPCR) demonstrated that circZYG11B expression was markedly increased during retinal neurodegeneration and . Cell Counting Kit‑8, TUNEL and caspase‑3 activity assays revealed that silencing of circZYG11B was able to protect against oxidative stress‑ or hypoxic stress‑induced retinal ganglion cell (RGC) injury. Furthermore, immunofluorescence staining and hematoxylin and eosin staining revealed that silencing of circZYG11B alleviated ischemia/reperfusion‑induced retinal neurodegeneration, as indicated by reduced RGC injury and decreased retinal reactive gliosis. In addition, luciferase reporter, biotin‑coupled miRNA capture and RNA immunoprecipitation assays revealed that circZYG11B could regulate RGC function through circZYG11B/microRNA‑620/PTEN signaling. Clinically, RT‑qPCR assays demonstrated that circZYG11B expression was markedly increased in the aqueous humor of patients with glaucoma. In conclusion, circZYG11B may be considered a promising target for the diagnosis and treatment of retinal ischemic diseases.
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http://dx.doi.org/10.3892/ijmm.2022.5162 | DOI Listing |
Exp Eye Res
January 2025
Department of Basic and Translational Science, Philadelphia, PA, 19104, United States; Department of Physiology, Philadelphia, PA, 19104, United States. Electronic address:
The P2X7 receptor (P2X7R) for extracellular ATP is implicated in several forms of retinal degeneration, including diabetic retinopathy, age-related macular degeneration, and glaucoma. P2X7R stimulation can trigger release of master cytokine IL-1β from microglia in the brain and from macrophages, but evidence of release from retinal microglia is indirect. Isolated mouse and rat retinal microglia, and wholemounts from CX3CR1 mice, were examined to determine if ATP induced IL-1β release directly from retinal microglial cells and if it also primed expression of IL-1β on an mRNA and protein level.
View Article and Find Full Text PDFMult Scler Relat Disord
January 2025
Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research, Biomedicine and Biomedical Engineering, University Hospital and University of Basel, Basel, Switzerland.
Background: People with MS show abnormal thinning of the retinal layers, which is associated with clinical disability and brain atrophy, and is a potential surrogate marker of neurodegeneration and treatment effects.
Objective: To evaluate the utility of retinal thickness as a surrogate marker of neurodegeneration and treatment effect in participants with secondary progressive MS (SPMS) from the optical coherence tomography (OCT) substudy of the EXPAND Phase 3 clinical trial (siponimod versus placebo).
Methods: In the OCT substudy population (n = 159), treatment effects on change in the average thickness of the retinal layer, peripapillary retinal nerve fiber layer (pRNFL), and combined macular ganglion cell and inner plexiform layers (GCIPL) were analyzed by high-definition spectral domain OCT at months 3, 12, and 24.
Surv Ophthalmol
January 2025
Department of Ophthalmology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania, United States. Electronic address:
Internal limiting membrane (ILM) peeling has been an acceptable step in vitrectomy surgeries for various retinal diseases such as macular hole, chronic macular edema following epiretinal membrane (ERM), and vitreoretinal traction. Despite all the benefits, this procedure has some side effects, which may lead to structural damage and functional vision loss. Light and dye toxicity may induce reversible and irreversible retina damage, which will be observed in postoperative optical coherence tomography scans.
View Article and Find Full Text PDFVision Res
January 2025
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Elevated intraocular pressure (IOP) is a significant risk factor for glaucoma, causing structural and functional damage to the eye. Increased IOP compromises the metabolic and structural integrity of retinal ganglion cell (RGC) axons, leading to progressive degeneration and influencing the ocular immune response. This study investigated early cellular and molecular changes in the retina and optic nerve (ON) following ocular hypertension (OHT).
View Article and Find Full Text PDFJCI Insight
January 2025
Gavin Herbert Eye Institute-Center for Translational Vision Research, Depar, University of California Irvine School of Medicine, Irvine, United States of America.
Elevation of intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction, leading to neurodegeneration, is the pathological hallmark of primary open-angle glaucoma (POAG). Impaired axonal transport is an early and critical feature of glaucomatous neurodegeneration. However, a robust mouse model that accurately replicates these human POAG features has been lacking.
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